We will determine whether high (325 meq NaCl/day) and moderately high (161 meq NaCl/day) salt intake causes increased blood pressure and sympathetic vascular tone in normotensive and 2-kidney one clip Goldblatt hypertensive dogs. Systemic arterial blood pressure (BP) and iliac or renal blood flow will be monitored while the animals are in a relaxed state. BP is taken through an implanted catheter and blood flow is measured with an electromagnetic flowmeter coupled to a flow probe on the iliac or renal artery. Sympathetic tone will be quantitated before and after high salt intake by the decrease in BP and iliac vascular resistance (IVR) caused by Alpha1-receptor blockade and the decrease in IVR produced by lumbar sympathetic nerve paralysis with procaine. Whether enhanced symphatetic tone caused by high salt diet is attributable to central or peripheral mechanism(s) will be a major objective of the study. Also, the possibility of a salt-induced effect on the kidney which then transmits a signal to the central nervous system to activate increased sympathetic outflow will be explored. Lastly, we will investigate the possibility that hypertension resulting from increased salt intake in normal and Goldblatt hypertensive dogs may be due in part to an increase in cardiac output. Our long-term objectives are to learn to what degree and for how long salt intake must be elevated above normal to cause deleterious cardiovascular effects and the mechanism of these effects.